medicine

OMG! I have now entered the Hell of the social consequences of “getting help” for a broken leg; not actually for the broken bones: (big cast boot; strict orders from the doc to not put any weight on that foot. Simple, really). I had been resisting mightily the “HOME HEALTH” industry; nice people who come to the house and take “vitals”- give baths (a quick swipe with a wash cloth) “do” physical therapy (whatever that is – undefined so far). “FREE” thanks to Medicare. But, they’re closed on weekends, use “restricted phone numbers” (caller can’t use caller ID or make return calls). WELL! Our nurses aren’t going to give out they’re phone numbers!” was the indignant reply when asked… Just call the ambulance, if you can’t reach us, although the fundamental idea of HOME HEALTH is to keep people OUT OF the Emergency Room.

I won’t / can’t go into the organizational structureof these services, because THERE IS NONE. The nurse just left (and left behind an enormous box of “free” medical supplies). I must have used the phrase “please be specific” a dozen times as she rambled on and on (vaguely) about services, service delivery, length (duration of services, determination of services available; that (for some unknown reason) the physical therapist is “master of all this “care” and why I need a social worker to “organize the experience”.

Actually, I shouldn’t have said there is no organizational structure:There are GOALS. 1. These are private companies, paid 100% by Medicare, so they will do / follow whatever bizarre and cockamamie “payment plan” that Congress has devised to ensure maximum profit for their “buddies” in the “helping, caring, fixing” industry. 2. This means setting up a “schedule” for myriad “employees” of HOME HEALTH to show up at times of their choosing (not based on need) – that is, a billable number of visits that stop immediately when Medicare stops. 3. Those “FREE” medical supply goodies are likely the most “high profit” stream: HOME HEALTH buys them in great bulk at pennies of the retail cost (say a roll of gauze, for $0.25) and bills Medicare $25.00…

In the end, I always ask myself,

Would I hire these people to do repairs and service on my truck? If not, why would I hire them to “work on” me?

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This is a story without end. Dozens of articles and studies argue over the number of deaths, which are “guessed at” “arrived at statistically” “reworked from archival material” “fudged” “denied” – in other words, the numbers have no reality – Why? Because data on medical deaths is not required on Death Certificates. There is no tracking of such deaths because they are not reported.

I wonder why? Could the Medical Industry be protecting itself by “not coming clean”?

Here’s where the public gets “shafted” Who would have guessed that the insurance industry is now dictating the content of Death Certificates, which are legal documents that affect each and every one of us, and which have widespread consequences for families tasked with the complex mysteries of navigating the post mortem experience, including cheap shots from insurance providers who refuse to live up to promised coverage.

In fact, the study, from doctors at Johns Hopkins, suggests medical errors may kill more people than lower respiratory diseases like emphysema and bronchitis do. That would make these medical mistakes the third leading cause of death in the United States. That would place medical errors right behind heart disease and cancer.

Through their analysis of four other studies examining death rate information, the doctors estimate there are at least 251,454 deaths due to medical errors annually in the United States. The authors believe the number is actually much higher, as home and nursing home deaths are not counted in that total.

This is a much greater number than a highly cited 1999 study from the Institute of Medicine that put the number in the 44,000 to 98,000 range. Other studies have put estimates closer to 195,000 deaths a year. The U.S. Department of Health and Human Services Office of the inspector general in 2008 reported 180,000 deaths by medical error among Medicare patients alone.

One reason there’s such a wide range of numbers is because accurate data on these kinds of deaths is surprisingly sparse. That’s in part because death certificates don’t ask for enough data, Makary said.

Currently the cause of death listed on the certificate has to line up with an insurance billing code. Those codes do not adequately capture human error or system factors.

“Billing codes are designed to maximize billing rather than capture medical errors,” Makary said.

So What is Self-Awareness Exactly? / The psychological study of self-awareness can be first traced back to 1972 when Psychologists Shelley Duval and Robert Wicklund developed the theory of self-awareness.

They proposed that: “when we focus our attention on ourselves, we evaluate and compare our current behavior to our internal standards and values. We become self-conscious as objective evaluators of ourselves.”

In essence, they consider self-awareness as a major mechanism of self-control.

Sounds pretty good; a state of “owning” one’s thoughts and intentions and the recognition that one’s behavior is often not congruent with these “values”. NOT the simple act of “mirror recognition” which belongs to the brain’s “visual system”.

Basic physical def: When you are awake and aware of your surroundings, that’s consciousness. (That “jives with” mirror recognition -type awareness as a property of an active sensory system).

The most influential modern physical theories of consciousness (there are supernatural theories, of course) are based on psychology and neuroscience. Theories proposed by neuroscientists such as Gerald Edelman and Antonio Damasio, and by philosophers such as Daniel Dennett, seek to explain consciousness in terms of neural events occurring within the brain. Consciousness – Wikipedia

It’s impossible here to present the long-standing and ever-growing confusion over the modern “concepts” of consciousness. It’s a word that is used for the most part, without any meaning whatsoever. Technology also has entered the arena.

My own idea is this…What we commonly refer to as “being consciousness” is a social interaction, an act of Co-consciousness; the product of language: “In Western cultures verbal language is inseparable from the process of creating a conscious human being.” see previous post: https://aspergerhuman.wordpress.com/?p=9198&preview=true

The computer, smartphone or other electronic device on which you are reading this article has a rudimentary brain—kind of.* (uh-oh. Pop-Sci)It has highly organized electrical circuits that store information and behave in specific, predictable ways, just like the interconnected cells in your brain.(No) On the most fundamental level, electrical circuits and neurons are made of the same stuff—atoms and their constituent elementary particles—but whereas the human brain is conscious, manmade gadgets do not know they exist.(WOW! NT nonsense!)Consciousness,most scientists argue, (made up assertion) is not a universal property of all matter in the universe. Rather, consciousness is restricted to a subset of animals with relatively complex brains. The more scientists study animal behavior and brain anatomy, however, the more universal consciousness seems to be. (Confused yet?)(Mirror awareness is a VISUAL phenomenon)

A brain as complex as the human brain is definitely not necessary for consciousness. (!!!)

On July 7 this year, a group of neuroscientists convening at Cambridge University signed a document officially declaring that non-human animals, “including all mammals and birds, and many other creatures, including octopuses” are conscious. (Well, that’s certainly proof that some poorly-defined experiential state in humans is a “thingy” also “in mammals and birds, and many other creatures, including octopuses” !!)

Humans are more than just conscious—they are also self-aware.Scientists differ on the difference between consciousness and self-awareness,(those imaginary Science Elves again, messing us up with “tricky” non specific definitions of “consciousness and self-awareness”) but here is onecommon explanation: Consciousness is awareness of one’s body and one’s environment; self-awareness is recognition of that consciousness—not only understanding that one exists, but further understanding that one is aware of one’s existence. Another way of thinking about it: To be conscious is to think; to be self-aware is to realize that you are a thinking being and to think about your thoughts.Presumably, human infants are conscious—they perceive and respond to people and things around them—but they are not yet self-aware. In their first years of life, infants develop a sense of self, learn to recognize themselves in the mirror(a phenomenon of the SENSORY SYSTEM) and to distinguish their own point of view from other people’s perspectives.

Notice how a lack of distinction / definition of terms leads to the inevitable “linear-causal-but-hierarchical arrangement of “notions” assumed to be correct (that is, how the brain works as an “isolated” command center, but which are “phrases” merely strung together by “social habit”.

Numerous neuroimaging studies have suggested that thinking about ourselves, recognizing images of ourselves and reflecting on our thoughts and feelings—that is, different forms self-awareness—all involve the cerebral cortex, the outermost, intricately wrinkled part of the brain. The fact that humans have a particularly large and wrinkly cerebral cortex relative to body size supposedly explains why we seem to be more self-aware than most other animals. (This pop-sci blah, blah is unforgivable in a “science” article.

One would expect, then, that a man missing huge portions of his cerebral cortex would lose at least some of his self-awareness. Patient R, also known as Roger, defies that expectation. Roger is a 57-year-old man who suffered extensive brain damage in 1980 after a severe bout of herpes simplex encephalitis—inflammation of the brain caused by the herpes virus. The disease destroyed most of Roger’s insular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex (mPFC), all brain regions thought to be essential for self-awareness. About 10 percent of his insula remains and only one percent of his ACC.

Note that “self-awareness” in this article is the “you are awake and aware of your surroundings” definition, and not the Duval, Wickland definition.

Roger cannot remember much of what happened to him between 1970 and 1980 and he has great difficulty forming new memories. He cannot taste or smell either. But he still knows who he is—he has a sense of self.He recognizes himself in the mirrorand in photographs.(This would indicate that his VISUAL system / memory is intact) To most people, Roger seems like a relatively typical man who does not act out of the ordinary.(That’s NTs for you; minimal evidence, inattentional blindness, social convention = “must be a normal person”) LOL

Carissa Philippi and David Rudrauf of the University of Iowa and their colleagues investigated the extent of Roger’s self-awareness in a series of tests. In a mirror recognition task, for example, a researcher pretended to brush something off of Roger’s nose with a tissue that concealed black eye shadow. 15 minutes later, the researcher asked Roger to look at himself in the mirror. Roger immediately rubbed away the black smudge on his nose and wondered aloud how it got there in the first place.

Philippi and Rudrauf also showed Roger photographs of himself, of people he knew and of strangers. He almost always recognized himself and never mistook someone else for himself, but he sometimes had difficulty recognizing a photo of his face when it appeared by itself on a black background, absent of hair and clothing. (Visual system)

Roger also distinguished the sensation of tickling himself from the feeling of someone else tickling him and consistently found the latter more stimulating. When one researcher asked for permission to tickler Roger’s armpits, he replied, “Got a towel?” As Philippi and Rudrauf note, Roger’s quick wit indicates that in addition to maintaining a sense of self, he adopts the perspective of others—a talent known as theory of mind.(Hmmm… a man without aninsular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex is capable of “mind-reading” and subtle social thinking and interaction. BUT, ASD Asperger people who have these “parts” intact, are not capable of “mind-reading” and social communication)He anticipated that the researcher would notice his sweaty armpits and used humor to preempt any awkwardness.

Just where is the “mythic social brain” located? In a textbook perhaps?

In another task, Roger had to use a computer mouse to drag a blue box from the center of a computer screen towards a green box in one of the corners of the screen. In some cases, the program gave him complete control over the blue box; in other cases, the program restricted his control. Roger easily discriminated between sessions in which he had full control and times when some other force was at work. In other words, he understood when he was and was not responsible for certain actions.(Aye, yai, yai. What a “stretchy” conclusion!) The results appear online August 22 in PLOS One.

Given the evidence of Roger’s largely intact self-awareness(visual recognition)despite his ravaged brain, Philippi, Rudrauf and their colleagues argue that the insular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex (mPFC) cannot by themselves account for conscious recognition of oneself as a thinking being. (Well, congratulations!) Instead, they propose that self-awareness is a far more diffuse cognitive process, relying on many parts of the brain, including regions not located in the cerebral cortex. (Why no recognition of VISUAL processing??)

In their new study, Philippi and Rudrauf point to a fascinating review of children with hydranencephaly—a rare disorder in which fluid-filled sacs replace the brain’s cerebral hemispheres. Children with hydranencphaly are essentially missing every part of their brain except the brainstem and cerebellum and a few other structures. Holding a light near such a child’s head illuminates the skull like a jack-o-lantern. Although many children with hydranencephaly appear relatively normal at birth, they often quickly develop growth problems, seizures and impaired vision. Most die within their first year of life. In some cases, however, children with hydranencephaly live for years or even decades. Such children lack a cerebral cortex—the part of the brain thought to be most important for consciousness and self-awareness—but, as the review paper makes clear, at least some hydranencephalic children give every appearance of genuine consciousness.They respond to people and things in their environment.When someone calls, they perk up. The children smile, laugh and cry. They know the difference between familiar people and strangers. They move themselves towards objects they desire. And they prefer some kinds of music over others. If some children with hydranencephaly are conscious, then the brain does not require an intact cerebral cortex to produce consciousness. (Which “consciousness” are we discussing?)

Hydranencephaly: “conscious” by definition “awake and aware of its surroundings” – there seems to be a consistent error in equating this definition (which is true of any animal that is not “asleep, dormant, anesthetized, or comatose” and includes automatic reflexes) and being aware that one is aware, or self-awareness).

Whether such children are truly self-aware, however, is more difficult to answer, especially as they cannot communicate with language. In D. Alan Shewmon‘s review, one child showed intense fascination with his reflection in a mirror (visual system), but it’s not clear whether he recognized his reflection as his own. Still, research on hydranencephaly and Roger’s case study indicate that self-awareness—this ostensibly sophisticated and unique cognitive process layered upon consciousness—might be more universal than we realized. (Totally ridiculous statement. Mixing simple visual recognition with Duval, Wickland definition. Still no clue as to what “consciousness” is.

References

Merker B (2007) Consciousness without a cerebral cortex: A challenge for neuroscience and medicine. Behavioral and Brain Sciences 30: 63-81.

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Pleiotropy: This certainly has implications for the endlessly repeated assertion that heritable genetic pathologies account for symptoms that include everything from “being antisocial” to “being interested in subjects that bore neurotypicals” to female ASDs “preferring to wear clothing with lots of pockets”. It is acknowledged that ASD / Asperger’s are a highly ‘heterogeneous’ bunch of individuals; no two are alike. Claims for “discovery” of scads of “autism-linked genes” are highly suspicious to begin with, and now this unsurprising report, in which “causal” links are over- and under- estimated, or MISSED COMPLETELY.

Source of Potential Bias Widespread in Large Genetic Studies

A new statistical method finds that many genetic variants used to determine trait-disease relationships may have additional effects that GWAS analyses don’t pick up.

By Diana Kwon | May 15, 2018

Genome-wide association studies, which scan thousands of genetic variants to identify links to a specific trait, have recently provided epidemiologists with a rich source of data. By applying Mendelian randomization, a technique that leverages an individual’s unique genetic variation to recreate randomized experiments, researchers have been able to infer the causal effect of specific risk factors on health outcomes, such as the link between elevated blood pressure and heart disease. (And all those supposed “links” between ASD / Autism “genes” and a bizarre selection / collection of “manifestations” in ASD / Asperger behavior, brain function and even in apparel choices)

The Mendelian randomization technique has long operated on the key assumption that horizontal pleiotropy, a phenomenon in which a single gene contributes to a disease through more than one pathway, is not happening. However, a new study published last month (April 23) in Nature Genetics finds that when it comes to potentially causal trait-disease relationships identified from genome-wide association studies (GWAS), pleiotropy is widespread—and may bias findings.

The “no pleiotropy” assumption was reasonable when scientists were examining only a few genes and much more was known about their specific biological functions, says Jack Bowden, a biostatistician at the University of Bristol’s MRC Integrative Epidemiology Unit in the U.K., who was not involved in the study. Nowadays, GWAS, which include many more genetic variants, are often conducted with little understanding about the precise mechanisms through which each gene could act on physiological traits, he adds.

Although researchers have suspected that pleiotropy exists in a large number of Mendelian randomization studies using GWAS datasets, “no one has actually tested how much of a problem this was,” says study coauthor Ron Do, a geneticist at the Icahn School of Medicine Mount Sinai.

To address this question, Do and his colleagues developed the so-called MR-PRESSO technique, an algorithm that identifies pleiotropy in Mendelian randomization analyses by searching for outliers in the relationship between the genetic variants’ effects on the trait of interest, say, blood pressure, and the same polymorphisms’ effects on the health outcome, such as heart disease. Outliers suggest that some genetic variants may not only be acting on the outcome through that particular trait—in other words, that pleiotropy exists.

The team used this method to test all possible trait-disease combinations generated from 82 publicly available GWAS datasets and found that pleiotropy was present in approximately 48 percent of the 191 statistically significant causal relationshipsthey identified.(Yes, statistics are only as good as the quality of the “thinking” of the people manipulating the process)

When the researchers compared the Mendelian randomization results before and after correcting for pleiotropy, they discovered that pleiotropy could lead to drastic over- or underestimations of the magnitude of a trait’s influence on a disease. (And ASD / Autism is NOT A DISEASE; it’s a collection of symptoms – which have multiple sources including WESTERN socio-cultural prejudice) Approximately 10 percent of the causal associations they found were significantly distorted, and by as much as 200 percent.

For example, the team identified an outlier variant in one of the significant causal relationships they found using Mendelian randomization—a link between body mass index (BMI) and levels of C-reactive protein, a marker for inflammation and heart disease. Further examination revealed that this variant, found in a gene encoding apolipoprotein E—a protein involved in metabolism—was associated with several traits and diseases, including BMI, C-reactive protein, cholesterol levels, and Alzheimer’s disease. After removing this outlier, the effect of BMI on C-reactive protein dropped by 12 percent, still statistically significant, but obviously to a lesser degree.

“There is growing awareness that there’s widespread pleiotropy in the human genome in general, and I think these findings suggest that there needs to be rigorous analysis and careful interpretation of casual relationships when performing Mendelian randomization,” (One would have thought that this was the conservative baseline in “science-based” research) Do says. “I think what’s going to have the biggest impact is not just saying whether causal relationships exist, but actually showing that the magnitude of the causal relationship can be distorted due to pleiotropy.”

Bowden notes that the presence of pleiotropy does not mean that Mendelian randomization is necessarily a flawed technique. “Many research groups around the world are currently developing novel statistical approaches that can detect and adjust for pleiotropy, enabling you to reliability test whether a [gene] has a causal effect on an outcome,” he tells The Scientist. For example, he and his colleagues at the University of Bristol recently reported another method to identify and correct for pleiotropy in large-scale Mendelian randomization analyses. (Are these “novel statistical approaches” proven to correct a problem that has much to do with the “reductive mindset” of those who place prime value on “any positive results” for their research agenda, above scientific discipline?)

“I hope that this paper will raise people’s attention to the potential problems in the assumptions behind [these studies],” says Wei Pan, a biostatistician at the University of Minnesota who was not involved in this work. “Large genetic datasets give researchers the opportunity to use a method like this to move the field forward, and as long as they use the method carefully, they can reach meaningful conclusions.” (Is this true, or social blah, blah?)

Pleiotropy:

The term pleiotropy is derived from the Greek words pleio, which means “many,” and tropic, which means “affecting.”Genes that affect multiple, apparently unrelated, phenotypes are thus called pleiotropic genes Pleiotropy should not be confused with polygenic traits, in which multiple genes converge to result in a single phenotype.

Examples of Pleiotropy

In some instances of pleiotropy, the influence of the single gene may be direct.For example, if a mouse is born blind due to any number of single-gene traits (Chang et al., 2002), it is not surprising that this mouse would also do poorly in visual learning tasks. In other instances, however, a single gene might be involved in multiple pathways. For instance, consider the amino acid tyrosine. This substance is needed for general protein synthesis, and it is also a precursor for several neurotransmitters (e.g., dopamine, norepinephrine), the hormone thyroxine, and the pigment melanin. Thus, mutations in any one of the genes that affect tyrosine synthesis or metabolism may affect multiple body systems. These and other instances in which a single gene affects multiple systems and therefore has widespread phenotypic effects are referred to as indirect or secondary pleiotropy (Grüneberg, 1938; Hodgkin, 1998).

Other examples of both direct and indirect pleiotropy are described in the sections that follow.

Chickens and the Frizzle Trait

In 1936, researchers Walter Landauer and Elizabeth Upham observed that chickens that expressed the dominant frizzle gene produced feathers that curled outward rather than lying flat against their bodies (Figure 2). However, this was not the only phenotypic effect of this gene — along with producing defective feathers, the frizzle gene caused the fowl to have abnormal body temperatures, higher metabolic and blood flow rates, and greater digestive capacity. Furthermore, chickens who had this allele also laid fewer eggs than their wild-type counterparts, further highlighting the pleiotropic nature of the frizzle gene.

As touched upon earlier in this article, there are many examples of pleiotropic genes in humans, some of which are associated with disease. For instance, Marfan syndrome is a disorder in humans in which one gene is responsible for a constellation of symptoms, including thinness, joint hypermobility, limb elongation, lens dislocation, and increased susceptibility to heart disease. Similarly, mutations in the gene that codes for transcription factor TBX5 cause the cardiac and limb defects of Holt-Oram syndrome, while mutation of the gene that codes for DNA damage repair protein NBS1 leads to microcephaly, immunodeficiency, and cancer predisposition in Nijmegen breakage syndrome.

One of the most widely cited examples of pleiotropy in humans is phenylketonuria (PKU). This disorder is caused by a deficiency of the enzyme phenylalanine hydroxylase, which is necessary to convert the essential amino acid phenylalanine to tyrosine. A defect in the single gene that codes for this enzyme therefore results in the multiple phenotypes associated with PKU, including mental retardation, eczema, and pigment defects that make affected individuals lighter skinned (Paul, 2000).

The phenotypic effects that single genes may impose in multiple systems often give us insight into the biological function of specific genes. Pleiotropic genes can also provide us valuable information regarding the evolution of different genes and gene families, as genes are “co-opted” for new purposes beyond what is believed to be their original function (Hodgkin, 1998). Quite simply, pleiotropy reflects the fact that most proteins have multiple roles in distinct cell types; thus, any genetic change that alters gene expression or function can potentially have wide-ranging effects in a variety of tissues.

Somewhat ironic, that large genetic studies REMOVE PLEIOTROPY, a “fact” in human genetics that may provide real progress in finding genetic links to physical conditions that are at present lumped together under a phony “autistic pathology” that is based in the “social brain” of neutrotypicals – and not in scientific reality.

A new study analyzing over 21,000 participants found that differences in activation of brain regions in different psychological “disorders” may have been overestimated, and confirms that there is still no brain scan capable of diagnosing a mental health concern.

A new study, published in the journal Human Brain Mapping, questions previous findings that specific brain regions are implicated in particular mental health conditions. Instead, according to the researchers, biased study design and the difficulty of publishing negative findings may have led to inaccurate results. While the researchers did find some differences in brain activation between people with mental health conditions and people without mental health conditions, they were not able to discriminate between specific diagnoses. The current study suggests that there are few, if any, differences in brain regions activated by specific mental health conditions. That is, there is still no brain scan that can tell whether a person has depression, social anxiety, or schizophrenia, for example.

Researchers have theorized that the different symptom clusters that form mental health diagnoses are linked to specific regions of the brain. If confirmed, such a finding would suggest that mental health diagnoses have biological components that could be targeted medically. However, the finding of the current study undermines this theory. Instead, the results indicate that while there is a general tendency for large parts of the brain (such as the amygdala and the hypothalamus) to be activated in a number of mental health conditions (as well as when humans are under stress in a number of ways), there is little difference between the varying diagnoses—even for diagnoses as seemingly different as social anxiety, depression, and schizophrenia.

The researchers were led by Emma Sprooten (Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York City). They used statistical tests to combine the results from 547 studies, which enabled them to analyze the data from 21,692 participants. The studies compared the brain scans of healthy participants with participants who were diagnosed with major depressive disorder, bipolar disorder, schizophrenia, obsessive compulsive disorder (OCD), and anxiety disorders, including social anxiety disorder, generalized anxiety disorder, panic disorder, specific phobias, and post-traumatic stress disorder (PTSD).

The studies in question used functional magnetic resonance imaging (fMRI), a common type of brain scan which creates images based on blood oxygenation levels within the brain. Higher blood oxygenation levels are assumed to indicate areas involved in more activity. Thus, an fMRI result is theorized to indicate which areas of the brain are activated or deactivated for particular tasks or states of being.

Importantly, fMRI has endured its own questions of bias. A recent article, published in the Proceedings of the National Academy of Sciences, confirmed a previous finding that up to 70% of the results in fMRI studies may actually be “false positives”—that is, finding a result when there actually is none. Nikos K. Logothetis wrote, in a 2008 article in Nature, that the fMRI “is an excellent tool for formulating intelligent, data-based hypotheses, but only in certain special cases can it be really useful for unambiguously selecting one of them, or for explaining the detailed neural mechanisms underlying the studied cognitive capacities.” That is, fMRI results can inform the questions we ask, but they can rarely answer those questions. Unfortunately, the neuropsychiatric literature is riddled with fMRI studies that purport to do just that.

Another recent study attempted to showcase just how much fMRI results rely on subjective interpretation. The researcher, Joshua Carp of the University of Michigan, examined a single fMRI event and found that there were 34,560 different results that could be reached by following different analysis procedures. He argues that the choice of analysis procedure is a subjective one, and researchers may try numerous procedures in order to achieve a positive result. He suggests that in the future, researchers must clearly specify which procedure they will use in order to reduce this extraordinary bias.

Sprooten and her colleagues framed their results as addressing the common practice of “reverse inference,” which has been challenged by other researchers as well. In reverse inference, researchers pre-select which brain regions (ROIs) they are going to study in order to maximize potential results—rather than examine the whole brain to determine which areas are activated. Put simply, if you study a particular area, then you will never see if there is activation in other brain regions during your test. You will only find activation in your pre-selected area. This result is often taken to indicate that particular disorders are associated with activation in particular regions—but this conclusion rests on the assumption that researchers would not have found other areas had they examined the whole brain.

The strength of the current study was its ability to compare ROI studies (studies that focused on only specific regions of the brain) with the results from whole-brain studies. The ROI studies tended to find differences in which brain regions were activated by different mental health conditions. However, once the whole-brain studies were factored in, these findings disappeared. When all studies were included, there were no differences between the diagnoses.

Notably, the researchers only included studies that found significant results—that is, those that purported to find differences between those with mental health diagnoses and those without. Their results would likely be even more striking if they factored in the studies with negative results—studies that did not find differences.

Sprooten writes:

“The pre-selection of ROIs, possibly in combination with the difficulty of publishing negative results, seems to bias the literature and may indirectly lead to oversimplification and over-localization of neurobiological models of behavior and symptoms.”

Choosing a brain region to examine, rather than examining the whole brain, appears to lead to biased, oversimplified results. Likewise, the conclusion that Logothetis reaches in his Nature article is that “the limitations of fMRI are not related to physics or poor engineering, and are unlikely to be resolved by increasing the sophistication and power of the scanners; they are instead due to the circuitry and functional organization of the brain, as well as to inappropriate experimental protocols that ignore this organization […]The magnitude of the fMRI signal cannot be quantified to reflect accurately differences between brain regions, or between tasks within the same region.”

The study conducted by Sprooten and her colleagues suggests that many fMRI studies misrepresent the abilities of brain scans. As Logothetis argues,

using fMRI results to confirm pre-existing theories of brain region activation in mental health diagnoses is in direct contradiction of the abilities of the fMRI technology.(It’s FRAUD!)

In short, brain scan research is of limited use in explaining the complex psychological states of human beings. If a neurological answer seems clear and easy, it may be being misrepresented and oversimplified.

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This post started as, “What is it with Asperger types and weather?” Lots of Aspies post / chat about weather sensitivities (me too), and the term “metabolism” often creeps in to the accounts. It’s apparent that few people know what metabolism is. I think that Aspies can benefit from “knowing how the body works” – I read all the time that everything from choice of breakfast cereal to what breed of cat to adopt is somehow linked to Asperger’s. Really?

Metabolism and weight loss: How you burn calories

Find out how metabolism affects weight, the truth behind slow metabolism and how to burn more calories.

You’ve probably heard people blame their weight on a slow metabolism, but what does that mean? Is metabolism really the culprit? And if so, is it possible to rev up your metabolism to burn more calories? It’s true that metabolism is linked to weight. But contrary to common belief, a slow metabolism is rarely the cause of excess weight gain. Although your metabolism influences your body’s basic energy needs, how much you eat and drink along with how much physical activity you get are the things that ultimately determine your weight.

Metabolism: Converting food into energy

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Metabolism is the process by which your body converts what you eat and drink into energy. During this complex biochemical process, calories in food and beverages are combined with oxygen to release the energy your body needs to function. Even when you’re at rest, your body needs energy for all its “hidden” functions, such as breathing, circulating blood, adjusting hormone levels, and growing and repairing cells. The number of calories your body uses to carry out these basic functions is known as your basal metabolic rate — what you might call metabolism.

In addition to your basal metabolic rate, two other factors determine how many calories your body burns each day:

Food processing (thermogenesis). Digesting, absorbing, transporting and storing the food you consume also takes calories. About 10 percent of the calories from the carbohydrates and protein you eat are used during the digestion and absorption of the food and nutrients.

Physical activity. Physical activity and exercise — such as playing tennis, walking to the store, chasing after the dog and any other movement — account for the rest of the calories your body burns up each day. Physical activity is by far the most variable of the factors that determine how many calories you burn each day.Scientists call the activity you do all day that isn’t deliberate exercise nonexercise activity thermogenesis (NEAT). This activity includes walking from room to room, activities such as gardening and even fidgeting. NEAT accounts for about 100 to 800 calories used daily.

The Total Crap that passes as American Wisdom. “Leo” Buscaglia PhD, also known as “Dr. Love,” was an American author and motivational speaker, and a professor in the Department of Special Education at the University of Southern California. Wikipedia

Metabolism and weight

It may be tempting to blame your metabolism for weight gain. But because metabolism is a natural process, your body has many mechanisms that regulate it to meet your individual needs. Only in rare cases do you get excessive weight gain from a medical problem that slows metabolism, such as Cushing’s syndrome or having an underactive thyroid gland (hypothyroidism).

Unfortunately, weight gain is a complicated process. It’s likely a combination of genetic makeup, hormonal controls, diet composition and the impact of environment on your lifestyle, including sleep, physical activity and stress.

All of these factors result in an imbalance in the energy equation. You gain weight when you eat more calories than you burn — or burn fewer calories than you eat. (Yes, it really is that simple!)

While it is true that some people seem to be able to lose weight more quickly and more easily than others, everyone loses weight when they burn up more calories than they eat. (Yes, it really is that simple.) To lose weight, you need to create an energy deficit by eating fewer calories or increasing the number of calories you burn through physical activity or both.

A closer look at physical activity and metabolism

While you don’t have much control over the speed of your basal metabolism, you can control how many calories you burn through your level of physical activity. The more active you are, the more calories you burn. In fact, some people who are said to have a fast metabolism are probably just more active — and maybe fidget more — than others.

You can burn more calories with: (Yes, it really is that simple)

Regular aerobic exercise. Aerobic exercise is the most efficient way to burn calories and includes activities such as walking, bicycling and swimming. As a general goal, include at least 30 minutes of physical activity in your daily routine.If you want to lose weight or meet specific fitness goals, you may need to increase the time you spend on physical activity even more. If you can’t set aside time for a longer workout, try 10-minute chunks of activity throughout the day. Remember, the more active you are, the greater the benefits.

Strength training. Experts recommend strength training exercises, such as weightlifting, at least twice a week. Strength training is important because it helps counteract muscle loss associated with aging. And since muscle tissue burns more calories than fat tissue does, muscle mass is a key factor in weight loss.

Lifestyle activities. Any extra movement helps burn calories. Look for ways to walk and move around a few minutes more each day than the day before. Taking the stairs more often and parking farther away at the store are simple ways to burn more calories. Even activities such as gardening, washing your car and housework burn calories and contribute to weight loss.

No magic bullet

Don’t look to dietary supplements for help in burning calories or weight loss. Products that claim to speed up your metabolism are often more hype than help, and some may cause undesirable or even dangerous side effects.

Dietary supplement manufacturers aren’t required by the Food and Drug Administration to prove that their products are safe or effective, so view these products with caution and skepticism. Always let your doctors know about any supplements you take.

There’s no easy way to lose weight. The foundation for weight loss continues to be based on physical activity and diet. Take in fewer calories than you burn, and you lose weight. (Yes, it really is that simple.)

The 2015 Dietary Guidelines for Americans recommends cutting calories by 500 to 700 calories a day to lose 1 to 1.5 pounds (0.5 to 0.7 kilograms) a week. If you can add some physical activity to your day, you’ll accomplish your weight-loss goals even faster.

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Google “Asperger’s and metabolism” or “Autism and metabolism” – you’ll find a load of blah, blah, blah … none of it conclusive; studies merely “suggest” an “association”, but no cause. All the weasel words so common in autism research are relied on for vague results and conclusions. Some people (a very tiny percentage of those designated as “autistic”) MAY have a metabolic problem, but this is usually connected to EPILEPSY. The usual backwards connections are made:some “thing” known as autism “causes” physiologic and behavioral problems, which are in fact, genetic or epigenetic changes, or known results of problem pregnancies; premature birth or disease / toxic conditions in the pregnant mother, or even damage to the fetus during botched deliveries. The vast majority (90-95%) of “autism cases” have no known cause, and yet, sweeping generalizations are emphatically made that “autism is a genetic, inherited disorder” Proof? NONE. Autism is not a disease, developmental disorder, genetic mutation, curse of god, ‘bad seed’ etc; it is a wildly incoherent list of symptoms (many are social judgements) cobbled together in a dreadfully prejudicial condemnation of “different” human behavior as “socially dangerous”.

Harris is the author of several books, and most recently edited Mental Disorders in the Classical World, published last summer. I spoke with him over email about how the ancient Greeks and Romans approached mental illness and what we can learn from them today.

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Could you start by explaining how attitudes toward mental illness were different in the classical world than they are today?xMany people in antiquity thought that mental disorders came from the gods. The Greek gods are a touchy lot, quick to take offense. For instance, they took a hard line with Orestes after his matricide. [Ed. Note: After killing his mother, Orestes was tormented by the Furies.] And in a world where many important phenomena such as mental illness were not readily explicable, the whims of the gods were the fallback explanation. Physicians and others fought against this idea from an early date (the 5th century B.C.), giving physiological explanations instead. Many people sought magical/religious remedies—such as going to spend the night in a temple of the healing god Asclepius, in the hope that he would work a cure or tell you how to get cured—[while physicians sought] mainly medical ones. No one thought that it was the duty of the state to care for the insane. Either their families looked after them, or they ended up on the street—a nightmare situation. (…that persists today. How far we’ve come as empathetic-compassionate modern social typicals…)xIn the introduction you wrote to Mental Disorders in the Classical World, you talk about “medicalizing mental illness.” When and why did people start to be seen as sick instead of crazy?xxx

Some time in the late 5th century B.C., some member of the school of Hippocrates wrote a treatise “On the Sacred Disease,” in which he argued that the “sacred disease,” i.e. epilepsy, was a physiological syndrome,and very soon all doctors and scientists (in so far as such a category existed) came to think that crazy people were sick (but not that they were not crazy).

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Greek doctors did not distinguish sharply between physical and mental disorders, and they did not have concepts that correspond simply with “depression” or “schizophrenia.” Roberto Lo Presti, in the book we are talking about, examines at length the development of Greek thinking about epilepsy. Greek doctors always tended to think that what we call psychoses were physiological in nature.xHow did doctors diagnose the mentally ill back then? What were the criteria they used? And how did they go about treating them?xThey were mostly (not entirely) concerned with psychoses (externalizing disorders such as antisocial personality disorder and drug and alcohol use disorders) rather than neuroses (internalizing disorders such as depression and anxiety), and they took into account a full range of hard-to-define symptoms including inappropriate behavior in public, delusions, delirium, and hallucinations. Treatments also covered a whole range from physical restraint to counseling; they did not make much use of pharmaceuticals.xIn the essay you contributed about hallucinations, you mention that in the classical world, people often saw gods and otherworldly things. Was there an evolution of hallucinations from being seen as a supernatural experience to as a symptom of something medically wrong?xThere was no simple evolution: the Hippocratic doctors already recognized hallucinations as a purely human phenomenon, but many ordinary people went on supposing that the gods were involved.xThe moral idea that anger was dangerous forms part of the widespread ancient idea that the essence of good behavior is self-control.x

Does this mean that hallucinations were more commonplace and less stigmatized than today?

No more commonplace, I think. Less stigmatized, yes, somewhat. One would not have sought treatment.

Socrates had hallucinations, right? Did that affect how he was perceived?

Socrates seems to have had recurrent hallucinations of one particular type: A voice spoke to him, usually advising him not to do things. His disciples were in awe of this phenomenon, but some of his later admirers thought they needed to explain it away—they thought it suggested that he was slightly cracked.

One of your older books is about rage—why was anger seen as an illness, or something to be controlled?

It took me about 400 pages to answer this question! Partly because it was seen as dangerous in the state, partly because it was seen as a danger in the family (especially because of slavery), partly later because excessive anger came to be seen as a personal moral failure.

Anger was dangerous to the state above all because it led to political violence, including tyrannical behavior by absolute rulers; dangerous to the family because of its potential to cause feuding and violence (as for slavery, the angry slave-owner could generally treat the slaves as he wished—but they might and did react). The moral idea arises out of these concrete political and social imperatives I think, but it also forms part of the widespread ancient idea that the essence of good behavior is self-control.

Are there difficulties applying today’s conceptions of what is “abnormal” to historical figures? Or vice versa?

There sure are, both ways. The conceptual and moral differences are huge.People have argued that, for example, Herod the Great and Caligula were schizophrenics, but tracing the way they actually behaved is rendered difficult by the inadequate sources [available]. And in the Roman world, a great deal of violence was normal, (as it is today) as was much of what we consider pedophilia. But this makes the work of scholars such as me more interesting as well as more difficult. (Child abuse and domestic violence are common today.)

Are there any ideas the ancient Greeks or Romans held that would be helpful for us to think about in the discussion surrounding mental illness today?

Yes, as far as neuroses are concerned, see in particular Chris Gill’s contribution
to the book I edited, with his emphasis on character. He looks at the idea that we should train our characters so that we are ready for life’s disasters and can face them robustly.